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Interferon-gamma prevents death of bystander neurons during CD8 T cell responses in the brain Richter K; Hausmann J; Staeheli PAm J Pathol 2009[May]; 174 (5): 1799-807T cells restricted to neurotropic viruses are potentially harmful as their activity may result in the destruction of neurons. In the Borna disease virus (BDV) model, antiviral CD8 T cells entering the brain of infected mice cause neurological disease but no substantial loss of neurons unless the animals lack interferon-gamma (IFN-gamma). We show here that glutamate receptor antagonists failed to prevent BDV-induced neuronal loss in IFN-gamma-deficient mice, suggesting that excitotoxicity resulting from glutamate receptor overstimulation is an unlikely explanation for the neuronal damage. Experiments with IFN-gamma-deficient mice lacking eosinophils indicated that these cells, which specifically accumulate in the infected brains of IFN-gamma-deficient mice, are not responsible for CA1 neuronal death. Interestingly, BDV-induced damage of CA1 neurons was reduced significantly in IFN-gamma-deficient mice lacking perforin, suggesting a key role for CD8 T cells in this pathological process. Specific death of hippocampal CA1 neurons could be triggered by adoptive transfer of BDV-specific CD8 T cells from IFN-gamma-deficient mice into uninfected mice that express transgene-encoded BDV antigen at high level in astrocytes. These results indicate that attack by CD8 T cells that cause the death of CA1 neurons might be directed toward regional astrocytes and that IFN-gamma protects vulnerable CA1 neurons from collateral damage resulting from exposure to potentially toxic substances generated as a result of CD8 T cell-mediated impairment of astrocyte function.|Adoptive Transfer[MESH]|Animals[MESH]|Apoptosis/*physiology[MESH]|Astrocytes/cytology/metabolism/pathology[MESH]|Borna Disease/metabolism/pathology/virology[MESH]|Borna disease virus/*physiology[MESH]|Brain/*immunology/metabolism/pathology[MESH]|CD8-Positive T-Lymphocytes/*immunology/metabolism/pathology[MESH]|Cytotoxicity, Immunologic[MESH]|Eosinophils/cytology/metabolism/pathology[MESH]|Female[MESH]|Flow Cytometry[MESH]|Hippocampus/cytology/metabolism/pathology[MESH]|Immunoenzyme Techniques[MESH]|In Situ Nick-End Labeling[MESH]|Inflammation[MESH]|Interferon-gamma/*physiology[MESH]|Lymphocytes/cytology/metabolism/pathology[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred BALB C[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Mice, Transgenic[MESH]|Neurons/*immunology/metabolism/pathology[MESH]|Perforin/metabolism[MESH]|Receptors, Glutamate/chemistry/metabolism[MESH]|Spleen/immunology/metabolism/pathology[MESH]|Viral Load[MESH] |
